Types of tympanostomy tubes and their names

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Here is a thorough breakdown of tympanostomy tube types:

Tympanostomy Tubes: Types and Names

Tympanostomy tubes (also called PE tubes, grommets, ventilation tubes, myringotomy tubes, or pressure equalization tubes) fall into two main categories based on how long they stay in the eardrum before extruding.

1. Short-Term Tubes (Grommet / Bobbin Design)

These are the most commonly used. They typically extrude spontaneously within 6-15 months. Most are shaped like a grommet or bobbin.

Name	Notes
Armstrong tube	One of the most widely used designs worldwide; about 80% extrude by 2 years. The Long Armstrong variant is least prone to early extrusion.
Shepard tube	Standard short-term grommet; fastest to extrude (~93% gone by 2 years in trials).
Paparella type I	Smaller inner flange; shorter retention than Paparella type II.
Reuter Bobbin	Cylindrical bobbin shape; 66% extruded by 2 years in one major RCT.
Donaldson tube	Double-flanged silicone design; studied against Armstrong in large trials.
Sheehy bobbin	Another popular bobbin-style short-term tube.

2. Long-Term Tubes (T-tube / Flanged Design)

Designed to stay in place for 15 months to several years. These have larger medial flanges or a T-shaped profile that resists extrusion. They are used in children with cleft palate, atrophic TM, or those who have already had multiple sets of short-term tubes.

Name	Notes
Goode T-tube	Classic T-shaped design; only 31% extruded by 2 years in randomized trials - the most retentive in head-to-head studies. Typically stays 3-5 years.
Paparella type II	Larger inner flange than type I; behaves as a long-term tube; associated with higher rates of persistent perforation after extrusion.
Per-Lee tube	Long-term flanged tube with wide inner flange.
Shah grommet	Modification of the grommet with larger inner flange for prolonged retention.
Collar button tube	Generic term for any tube shaped like a collar button (wide inner flange, narrow shaft).

Key Structural Variables That Affect Tube Behavior

Shape of the medial flange - larger flanges resist extrusion (longer retention).
Lateral flange presence - absence of a lateral flange speeds extrusion.
Shaft length and inner diameter - affects patency and drainage.
Material - most modern tubes are fluoroplastic (PTFE) or silicone, replacing older stainless steel, titanium, and gold tubes. Silicone tubes are associated with the longest time to first infection.

Summary: Short-Term vs. Long-Term at a Glance

Feature	Short-Term (Grommet)	Long-Term (T-tube)
Retention	6-15 months	15 months to several years
Extrusion	Spontaneous	Often needs surgical removal
Best for	Most children with OME/rAOM	Cleft palate, atrophic TM, failed prior tubes
Examples	Armstrong, Shepard, Reuter Bobbin, Donaldson	Goode T-tube, Per-Lee, Paparella II

Source: Cummings Otolaryngology Head and Neck Surgery (textbook, "Types of Tympanostomy Tubes and Indications") and Wikipedia on tympanostomy tubes. A 2020 SAGE visual guide specifically lists Armstrong II, Paparella I, Donaldson, Shepard, Sheehy, and Reuter Bobbins as the dominant short-term tubes worldwide.

Physiology of balance and tests of vestibular system

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Physiology of Balance and Tests of the Vestibular System

Part 1: Physiology of Balance

The Three Sensory Inputs

Balance ("postural equilibrium") is maintained by integrating three sensory systems in the brainstem and cerebellum:

Vestibular system - detects head motion and gravity
Visual system - provides spatial orientation cues
Proprioceptive / somatosensory system - joint and muscle position sense from the periphery

Disruption of any one of these can be partially compensated by the other two. When two or more are impaired, significant imbalance results.

Anatomy of the Vestibular End Organ

The vestibular apparatus sits within the bony labyrinth of the temporal bone, adjacent to the cochlea. It consists of a membranous labyrinth filled with endolymph and surrounded by perilymph.

Structures of the vestibular organ showing the three semicircular canals (superior, posterior, horizontal), utricle, saccule, and ampullae

Fig. Structures of the vestibular organ - Costanzo Physiology 7th Ed.

It has five end organs in each ear:

Structure	Number	Detects
Semicircular canals (SCCs)	3 (horizontal, superior, posterior)	Angular / rotational acceleration
Utricle	1	Linear acceleration (horizontal plane)
Saccule	1	Linear acceleration (vertical plane, gravity)

Semicircular Canals - How They Work

The three SCCs are arranged perpendicular to one another, covering all three axes of head rotation. Each canal has an ampulla at one end containing vestibular hair cells embedded in a gelatinous mass called the cupula. The cupula spans the entire cross-section of the ampulla and has the same specific gravity as endolymph.

Mechanism of transduction: When the head rotates, the bony canal and attached ampulla move, but the endolymph initially lags due to inertia. This relative movement deflects the cupula, bending the stereocilia on hair cells.

Vestibular hair cell structure and function during counterclockwise head rotation, showing depolarization (excitation) of left canal and hyperpolarization (inhibition) of right canal

Fig. Vestibular hair cell transduction - Costanzo Physiology 7th Ed.

Stereocilia bent toward the kinocilium → hair cell depolarizes → increased afferent firing
Stereocilia bent away from kinocilium → hair cell hyperpolarizes → decreased afferent firing

Push-pull pairing: The lateral SCCs are paired with each other; the left superior SCC pairs with the right posterior SCC, and vice versa. When the head moves, one canal in a pair is excited while the opposite is inhibited. The CNS reads the differential firing rate as the signal for head movement.

"Hair cells within the SCCs fire at a baseline rate when at rest. When the head is moved rotationally, one of the pair of canals will increase its firing rate while the other will decrease. This differential signals a head movement in the plane of that canal." - K.J. Lee's Essential Otolaryngology

Otolith Organs - Utricle and Saccule

These detect linear acceleration (including gravity). Within them, the macula contains hair cells covered by an otolith mass - a gelatinous membrane embedded with calcium carbonate crystals (otoconia).

When the head tilts, gravity pulls the heavy otolith mass across the hair cells, bending stereocilia
Utricle: macula oriented horizontally when upright; detects lateral tilt and forward/backward linear motion
Saccule: macula oriented vertically when upright; detects up/down motion (pitch and roll)

Because of the bilateral arrangement, every possible head orientation produces a unique pattern of excitation/inhibition across the four otolith organs (2 utricles + 2 saccules).

Central Vestibular Pathways

Afferent fibers from hair cells travel in the vestibular division of CN VIII to four vestibular nuclei in the medulla:

Nucleus	Main Input	Main Output
Superior	SCCs	Extraocular muscles via MLF (mediates VOR)
Medial	SCCs	Extraocular muscles via MLF
Lateral (Deiters)	Utricle	Spinal cord via lateral vestibulospinal tract (postural reflexes)
Inferior	SCCs + otoliths	Brainstem + cerebellum via MLF

The cerebellum modulates and fine-tunes all vestibular signals.

Vestibulo-Ocular Reflex (VOR)

The VOR maintains stable gaze during head movement. It generates eye movements equal and opposite to head rotation, preventing "retinal slip." The fovea covers a small visual field and cannot be kept on target by voluntary pursuit alone - the VOR fills this role during rapid head movements.

Normal VOR: head turns right → eyes move left at equal velocity → gaze remains stable
Impaired VOR (e.g., unilateral vestibular loss): head turns toward the affected side → eyes fail to compensate → a catch-up saccade is seen (the basis of the head impulse test)

Nystagmus - the hallmark of vestibular activity - consists of:

Slow phase: the compensatory eye drift driven by vestibular input
Fast phase (saccade): the rapid "reset" movement; nystagmus is named by the direction of the fast phase

Part 2: Tests of the Vestibular System

A. Bedside / Clinical Tests

Test	What It Tests	How Done	Interpretation
Dix-Hallpike maneuver	Posterior SCC (BPPV)	Patient moved rapidly from sitting to head-hanging position, head turned 45°; Frenzel lenses improve sensitivity	Torsional upbeat nystagmus with latency, fatigability = BPPV; persistent/non-fatiguing = central
Head Impulse Test (HIT)	High-frequency VOR (horizontal SCC)	Examiner grasps head, makes a small rapid unpredictable head thrust; patient fixes on examiner's nose	Corrective saccade after the thrust = ipsilateral canal paresis (peripheral); normal VOR + nystagmus + skew deviation = HINTS criteria for central lesion
Romberg test	Postural control + proprioception	Stand feet together, arms crossed, eyes closed	Falling/excessive sway = peripheral vestibular, cerebellar, or severe neuropathy; does not localize on its own
Fukuda Stepping Test	Peripheral labyrinthine function	March in place 50 steps, eyes closed, arms outstretched	Rotation >45° = peripheral vestibular weakness; most sensitive for severe unilateral dysfunction
Unterberger test	Similar to Fukuda	Arms horizontal, eyes closed, march 50 steps	Rotation toward side of lesion
Skew deviation	Otolith-ocular pathway integrity	Cover-uncover test; look for vertical correction of each eye alternately	Skew (vertical misalignment) = brainstem/cerebellar lesion

B. Laboratory / Instrumental Tests

1. Electronystagmography / Videonystagmography (ENG/VNG)

The most widely used formal vestibular test battery.

ENG: records eye movements indirectly via electrodes measuring the corneoretinal potential (dipole). Electrodes placed at lateral canthi and around one eye.
VNG: records directly with infrared video cameras in real time.

Test subsets:

Vestibular subsets:

Spontaneous nystagmus
Gaze nystagmus
Positional nystagmus
Positioning (Dix-Hallpike) nystagmus
Fistula test
Bithermal caloric tests

Oculomotor subsets:

Smooth pursuit
Saccadic system
Optokinetic system
Fixation suppression

2. Bithermal Caloric Test

The most important component of ENG/VNG - it tests the lateral SCC of each ear independently.

Setup: Head tilted back 60° (so horizontal canals are vertical). Each ear irrigated separately with:

Water: 44°C (warm) and 30°C (cool) for 30 seconds each
Air: 58°C and 24°C for 60 seconds (used when TM is perforated)

Mechanism: Temperature creates a convection current in endolymph - either ampullopetal (toward ampulla) or ampullofugal (away) flow - mimicking head rotation.

Mnemonic: COWS (Cold Opposite, Warm Same)

Cold water → endolymph drops → ampullofugal flow → inhibition → nystagmus to the Opposite side
Warm water → endolymph rises → ampullopetal flow → excitation → nystagmus to the Same side

Calculations:

Unilateral weakness (UW) = [(RW + RC) - (LW + LC)] / (RW + RC + LW + LC) × 100%
- 15-30% = abnormal (peripheral lesion on the weaker side)
Directional preponderance (DP) = comparison of right-beating vs. left-beating responses
- 30% may suggest central lesion
Bilateral weakness: total slow-phase velocity for each side <12°/s

Contraindication: water irrigation with TM perforation (use air instead)

Central vs. Peripheral ENG findings:

Peripheral Signs	Central Signs
Unilateral caloric weakness	Spontaneous nystagmus with normal calorics
Bilateral weakness with known ototoxicity	Direction-changing nystagmus
Fatiguing positional nystagmus	Failure of fixation suppression
Direction-fixed nystagmus	Abnormal saccades with normal calorics
Intact fixation suppression	Hyperactive caloric responses

3. Rotary Chair Test (Rotational Chair / Sinusoidal Harmonic Acceleration)

Patient sits in a motorized chair rotating in darkness at various frequencies
Tests the VOR across a range of stimulus frequencies
Tests both labyrinths simultaneously - useful when calorics are inconclusive
Key parameters: VOR gain, phase, and symmetry
Phase leads at low frequencies indicate loss of velocity storage (sign of peripheral lesion)

4. Vestibular Evoked Myogenic Potentials (VEMPs)

cVEMP (cervical VEMP): loud sound stimulus → saccule → inferior vestibular nerve → ipsilateral sternocleidomastoid inhibition. Tests saccule and inferior vestibular nerve.
oVEMP (ocular VEMP): same stimulus → utricle → superior vestibular nerve → contralateral inferior oblique activation. Tests utricle and superior vestibular nerve.
Useful for diagnosing superior semicircular canal dehiscence, vestibular neuritis, and Meniere's disease.

5. Video Head Impulse Test (vHIT)

Modern, objective version of the bedside HIT
High-speed infrared camera tracks eye movements during rapid head thrusts in all six SCC planes
Quantifies VOR gain for each individual SCC
Detects covert saccades invisible to the naked eye

6. Computerized Dynamic Posturography (CDP)

Measures postural stability on a moving platform while visual and/or proprioceptive cues are manipulated
The sensory organization test (SOT) isolates each sensory input systematically
Useful for functional assessment, rehab planning, and disability evaluation

7. Bárány (Rotation) Test - Historical/Bedside

Rotating the patient ~10 revolutions in a special chair then stopping abruptly:

Normal: post-rotatory nystagmus toward the opposite side; patient falls toward the side of original rotation
Tests both labyrinths simultaneously

Summary Table: Tests at a Glance

Test	Structure Tested	Key Feature
Dix-Hallpike	Posterior SCC (BPPV)	Latency + fatigability = peripheral
Head Impulse (HIT/vHIT)	Horizontal SCC, high-frequency VOR	Catch-up saccade = ipsilateral paresis
Romberg	Postural control, proprioception	Non-localizing
Fukuda stepping	Peripheral labyrinth	>45° turn = peripheral deficit
ENG/VNG + Calorics	Each lateral SCC independently	COWS mnemonic; best for side-of-lesion
Rotary chair	Both labyrinths, VOR gain/phase	Best for bilateral loss assessment
cVEMP	Saccule + inferior vestibular nerve	Ipsilateral SCM inhibition
oVEMP	Utricle + superior vestibular nerve	Contralateral inferior oblique activation
CDP/Posturography	All three balance inputs	Functional disability, rehab

Sources: Costanzo Physiology 7th Ed. (pp. 102-104); K.J. Lee's Essential Otolaryngology (pp. 345-352); Cummings Otolaryngology Head and Neck Surgery (p. 2638); Scott-Brown's Otorhinolaryngology Vol. 2

Rhinolith

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Rhinolith (Nasal Calculus / Rhinolithiasis)

Definition

A rhinolith (from Greek rhinos = nose + lithos = stone) is a calcified concretion - a mineral stone - that forms within the nasal cavity. The condition is called rhinolithiasis. It was first described by Bertholin in 1654 and remains a rare but clinically important cause of unilateral nasal obstruction.

Pathogenesis

Formation occurs in three overlapping stages:

1. Nidus Formation

A nidus (central core) must be present to initiate mineralization. Nidi are classified as:

Type	Examples
Endogenous	Bone fragment, ectopic dental tissue (odontoma), blood clot, nasal epithelial debris, inspissated secretions
Exogenous	Fruit seeds, buttons, rubber, paper, cotton wool, beads, sponge, battery fragments

2. Mineralization

Mineral salts from nasal secretions, blood, and inflammatory exudate deposit around the nidus in concentric layers. The minerals involved are:

Calcium phosphate (primary)
Calcium carbonate
Magnesium phosphate and carbonate

3. Mucosal Erosion and Growth

As the hard calcified capsule enlarges, it erodes the surrounding nasal mucosa, triggers chronic inflammation, and progressively obstructs the nasal airway. This process is very slow - stones can grow silently for years or even decades (one case report documented a rhinolith in situ for over 80 years).

Contributing factors: nasal septal deviation, bone spurs, and impaired mucociliary clearance - all promote stagnation of debris that acts as a holding platform for precipitation.

Location

Usually unilateral, found in the anterior nasal cavity
Most common sites: around the inferior turbinate and against the nasal septum
No consistent predilection for left vs. right side

Clinical Features

Symptoms depend on the size of the stone. Small rhinoliths are often completely asymptomatic and discovered incidentally on imaging.

Once large enough, the classic presentation is:

Feature	Details
Unilateral nasal obstruction	Most common complaint (~71%); chronic, resistant to medical treatment
Foul-smelling (malodorous) discharge	Purulent, unilateral rhinorrhea - due to surrounding mucosal necrosis and secondary infection
Epistaxis	~17% of cases - from erosion of mucosa
Headache / facial pain	~17%
Anosmia	From obstruction
Epiphora	If obstruction involves the nasolacrimal duct

The classic triad to suspect rhinolith: chronic unilateral nasal obstruction + foul-smelling unilateral discharge + failure to respond to antibiotics

Diagnosis

1. Anterior Rhinoscopy

May reveal a hard, irregular, grayish-brown or yellowish mass in the nasal cavity
Stone may be partially covered by granulation tissue or crusts

2. Rigid Nasal Endoscopy

Confirms diagnosis, localizes the stone
Allows visualization of associated mucosal pathology
May enable direct extraction in accessible cases

3. Radiology

X-ray (plain film): rhinoliths are radio-opaque (due to calcium/magnesium salts); may be seen on a lateral skull or water's view
CT scan (gold standard): shows a hyperdense mass with a hypodense center (the organic nidus). CT:
- Accurately maps size and location
- Identifies complications (sinusitis, erosion into adjacent structures)
- Excludes differentials

Differential Diagnosis

Condition	Distinguishing Feature
Nasal foreign body (non-calcified)	Radiolucent on plain film
Calcified nasal polyp	History of polyps; usually not centered on a discrete nidus
Odontoma / ectopic tooth	CT and dental review
Osteoma	Arises from bone, uniformly dense
Chondrosarcoma	Aggressive features, soft tissue component
Granulomatous disease (Wegener's, TB, syphilis)	Systemic features, serology
Fibrous dysplasia	Ground-glass appearance on CT, involves bone

Complications (if untreated)

Due to progressive mucosal erosion and secondary infection, untreated rhinoliths can cause:

Sinusitis (most common)
Septal perforation
Nasal deformity
Orbital cellulitis / palpebral abscess
Frontal osteomyelitis
Meningitis / epidural abscess (rare, serious)
Hypoplasia of the inferior turbinate (from chronic pressure)

Treatment

Surgical removal is the definitive treatment. Options include:

Approach	Indication
Anterior rhinoscopy / office removal	Small, accessible stones - hook or Jobson Horne probe placed behind stone, pulled forward
Rigid nasal endoscopy (FESS)	Most cases; allows visualization + precise removal; stone fragmented if too large
Trans-oral (nasopharyngeal) approach	Large stones pushed posteriorly into nasopharynx under GA
Fogarty balloon catheter	Balloon passed behind stone, inflated, pulled forward
"Mother's kiss" technique	Children; mouth-to-mouth blow with opposite nostril occluded - effective in ~60% of foreign bodies

Practical points:

Large rhinoliths may need to be fragmented in situ before removal
Histopathological examination of the removed stone is mandatory - to identify the nidus and rule out neoplasia
Post-removal: treat any underlying sinusitis; nasal douching

Key Facts Summary

Feature	Details
First described	Bertholin, 1654
Composition	Calcium + magnesium phosphate and carbonate salts
Radiological appearance	Radio-opaque; CT: hyperdense with hypodense center
Classic triad	Unilateral obstruction + foul discharge + treatment failure
Gold standard imaging	CT scan
Treatment	Endoscopic surgical removal
Histology	Always send for pathological examination

Sources: Scott-Brown's Otorhinolaryngology Head & Neck Surgery Vol. 2; K.J. Lee's Essential Otolaryngology; KBB-Forum clinical study on rhinolith; Rhinolithiasis - OAText case report

Rhinolith

I just covered Rhinolith in detail in my previous response. Here's a concise summary of everything discussed:

Rhinolith - Quick Reference

Definition: A calcified stone (nasal calculus) forming within the nasal cavity around a central nidus. First described by Bertholin (1654).

Nidus Types

Endogenous	Exogenous
Bone fragment, ectopic tooth, blood clot, epithelial debris	Fruit seed, button, rubber, paper, cotton wool

Composition

Salts of calcium phosphate, calcium carbonate, magnesium phosphate and carbonate - making it radio-opaque.

Classic Triad

Chronic unilateral nasal obstruction
Foul-smelling unilateral purulent discharge
Failure to respond to antibiotics/medical treatment

Other Symptoms

Epistaxis (~17%)
Headache / facial pain (~17%)
Anosmia, epiphora

Diagnosis

Anterior rhinoscopy: hard grayish-brown/yellowish mass
Rigid nasal endoscopy: confirms + localizes
Plain X-ray: radio-opaque shadow
CT scan (gold standard): hyperdense mass with hypodense center (the nidus)

Differentials

Nasal foreign body, osteoma, calcified polyp, odontoma, granulomatous disease (Wegener's, TB), fibrous dysplasia, chondrosarcoma

Complications (if untreated)

Sinusitis → septal perforation → nasal deformity → orbital cellulitis → frontal osteomyelitis → meningitis / epidural abscess

Treatment

Small/accessible: office removal with hook or Jobson Horne probe
Most cases: rigid nasal endoscopic removal (fragment in situ if large)
Very large: pushed into nasopharynx and removed trans-orally under GA
Always send for histopathological examination

If you'd like me to go deeper into any specific aspect - pathogenesis, imaging findings, surgical technique, or differentials - just let me know.

Oesophagus anatomy and Oesophagus motility disorders

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Excellent - I now have rich textbook material across anatomy, histology, innervation, blood supply, and all major motility disorders. Let me compile the full response.

Oesophagus - Anatomy and Motility Disorders

PART 1: ANATOMY OF THE OESOPHAGUS

General Description

The oesophagus is an 18-26 cm long, flattened muscular tube - the immediate continuation of the pharynx - that connects the lower border of the cricoid cartilage (C6) to the cardiac orifice of the stomach (T11). It is the narrowest part of the digestive tract (excluding the appendix). Between swallows it lies collapsed, but can distend up to 2 cm anteroposteriorly and 3 cm laterally to accommodate a bolus.

Divisions

Division	Vertebral Level	Length from Incisors
Cervical	C6 - T1	15-18 cm
Thoracic	T1 - T10	18-38 cm
Abdominal	T10 - T11	38-40 cm

The oesophagus is not a straight tube - it deviates laterally at several points:

In the neck: veers left from midline
At T5: returns to midline, then veers left again
At T7: continues left until it pierces the diaphragm

It also follows the anteroposterior curvature of the vertebral column.

Anatomical Constrictions

There are three (or four) constrictions, important for understanding where foreign bodies lodge, strictures form, and where rigid oesophagoscopy is most hazardous:

Constriction	Cause	Distance from Incisors
1st - Cricopharyngeal	Cricopharyngeus (UES) - narrowest point	~15 cm
2nd - Aortic	Arch of the aorta crosses over	~22 cm
3rd - Bronchial	Left main bronchus crosses over	~27 cm
4th - Diaphragmatic	Oesophageal hiatus of diaphragm	~38 cm

The aortic and bronchial constrictions are often grouped together as a single "bronchoaortic" constriction.

Relations of Each Segment

Cervical Oesophagus:

Anterior: trachea (connected by loose areolar tissue)
Posterior: vertebral column (C6-C7), prevertebral fascia, longus colli muscle
Lateral: common carotid arteries (in carotid sheaths), lower poles of thyroid gland
Left: thoracic duct (ascending portion)
Grooves between trachea and oesophagus: recurrent laryngeal nerves (surgically critical)

Thoracic Oesophagus:

In the superior mediastinum:

Anterior: trachea, left recurrent laryngeal nerve
Left lateral: aortic arch, left subclavian vein, thoracic duct, left pleura
Posterior: T1-T4 vertebral bodies

In the posterior mediastinum (inferior mediastinum):

Anterior: left main bronchus, tracheobronchial nodes, pericardium, left atrium
Right: azygos vein, mediastinal pleura
Left: descending aorta (until oesophagus crosses anterior to it near T10)
Posterior: thoracic duct (crosses from right to left at T5), hemiazygos veins
The vagus nerves form a plexus around the oesophagus here

Abdominal Oesophagus:

Only ~2 cm long
Lies in the oesophageal groove on the posterior surface of the left lobe of the liver
Enclosed by the phrenoesophageal ligament

Histological Layers

The oesophageal wall has four layers (unlike the rest of the GI tract, it has no serosa):

Layer	Key Features
Mucosa	Stratified squamous non-keratinizing epithelium; transitions to columnar at the Z-line (squamocolumnar junction / gastro-oesophageal junction)
Submucosa	Dense connective tissue; contains blood vessels, lymphatics, Meissner (submucosal) plexus, and oesophageal mucous glands (secrete mucus, bicarbonate, EGF for protection)
Muscularis propria	Inner circular + outer longitudinal layers; Auerbach (myenteric) plexus between them
Adventitia	Loose connective tissue - no serosa (this is why oesophageal cancer spreads so readily to adjacent structures)

Muscle composition along the length:

Upper 5-33%: skeletal muscle only
Middle third: mixed skeletal and smooth muscle
Lower 50%: smooth muscle only

Sphincters

Upper Oesophageal Sphincter (UES):

Formed mainly by the cricopharyngeus muscle + inferior pharyngeal constrictor
Skeletal muscle; contracted at rest (~60-100 mmHg)
Prevents air entering the oesophagus during inspiration
Relaxes reflexly during swallowing

Lower Oesophageal Sphincter (LES):

2-4 cm of asymmetrically thickened circular smooth muscle just above the gastro-oesophageal junction
Resting pressure: ~15-30 mmHg
Maintained by tonic contraction + diaphragmatic crural contraction during inspiration
Fixed in position by the phrenoesophageal ligament (from transversalis fascia of diaphragm)
Relaxes during swallowing to allow bolus to enter the stomach

Innervation

Motor (efferent):

Skeletal muscle (upper oesophagus): vagal postganglionic fibers from the nucleus ambiguus terminate directly on motor endplates
Smooth muscle (lower oesophagus): vagal preganglionic fibers from the dorsal motor nucleus synapse on neurons of Auerbach's (myenteric) plexus
Sympathetic: from thoracic sympathetic chain (T5-T12) - reduces peristalsis

Sensory (afferent):

Meissner plexus (submucosal) collects sensory signals
Pain via chemoreceptors (mucosa/submucosa) and mechanoreceptors (musculature)
Vagal afferents → nodose ganglia → nucleus tractus solitarius in medulla
Sympathetic afferents → dorsal root ganglia → dorsal horn → spinothalamic/spinoreticular tracts → thalamus → somatosensory cortex

Because oesophageal neuroanatomic pathways overlap with those of the heart and respiratory system, chest pain from oesophageal disease is clinically indistinguishable from cardiac pain.

Blood Supply

Segmental arterial supply:

Segment	Artery
Cervical	Branches of inferior thyroid artery
Upper thoracic	Bronchial arteries
Mid thoracic	Direct branches from descending thoracic aorta
Lower thoracic/abdominal	Left gastric artery + left inferior phrenic artery

Venous drainage:

Cervical → inferior thyroid veins → brachiocephalic veins
Thoracic → azygos / hemiazygos veins
Abdominal → left gastric (coronary) vein → portal system
The abdominal oesophageal veins form a portosystemic anastomosis - dilate as oesophageal varices in portal hypertension

Lymphatic drainage:

Cervical oesophagus → deep cervical nodes
Thoracic → posterior mediastinal nodes
Abdominal → left gastric / coeliac nodes
Note: submucosal lymphatics run longitudinally for several centimetres before penetrating the muscle coat - explains skip metastases in oesophageal cancer

PART 2: OESOPHAGEAL MOTILITY DISORDERS

"Esophageal motility disorders are diseases attributable to abnormal esophageal neuromuscular dysfunction commonly associated with dysphagia, chest pain, or heartburn." - Harrison's Principles of Internal Medicine 22e

The major primary disorders are: Achalasia, Distal Oesophageal Spasm (DES), and Hypercontractile (Jackhammer) Oesophagus. Secondary motility disorders include those from systemic disease.

Diagnostic Tools

Test	What It Shows
High-resolution manometry (HRM)	Gold standard; measures pressure along entire oesophagus; classifies disorders by Chicago Classification
Barium swallow	Structural assessment; detects dilatation, tapering, corkscrew pattern
Endoscopy	Excludes structural / inflammatory disease
CT / EUS	Rules out pseudoachalasia from extrinsic tumour

1. Achalasia

The prototypic and most common primary oesophageal motility disorder.

Incidence: 1-3 per 100,000; peak age 25-60 years

Pathophysiology:

Autoimmune-mediated degeneration of ganglion cells in the myenteric plexus → aganglionosis
Both excitatory (cholinergic) and inhibitory (nitric oxide-mediated) neurons are lost
The inhibitory neurons mediate LES relaxation and sequential peristalsis propagation
Net result: absent peristalsis + impaired LES relaxation
Possible trigger: latent HSV-1 infection + genetic susceptibility

Pathological Triad (Robbins):

Incomplete LES relaxation
Increased LES tone
Aperistalsis (absent peristalsis) of the oesophageal body

Clinical Features:

Dysphagia to both solids AND liquids (differentiates from mechanical obstruction)
Regurgitation of undigested food/secretions
Chest pain - squeezing, pressure-like, may radiate to neck/arms/jaw
Weight loss
Respiratory complications: aspiration bronchitis, pneumonia, lung abscess
Some patients complain of paradoxical "heartburn"

Barium Swallow Appearance:

Dilated oesophagus with poor emptying
Air-fluid level
"Bird-beak" or "rat-tail" tapering at the LES

Achalasia barium swallow showing dilated oesophagus with tapering at the gastroesophageal junction and air-fluid level; right image shows sigmoid deformity in advanced disease

Barium swallow in achalasia: bird-beak tapering at LES (right) and sigmoid deformity in advanced disease (left) - Harrison's Principles of Internal Medicine 22e

High-Resolution Manometry - Three Subtypes (Chicago Classification):

High-resolution manometry showing three subtypes of achalasia: A. Classic (minimal oesophageal pressurisation), B. Achalasia with oesophageal compression (pan-oesophageal pressurisation), C. Spastic achalasia (spastic contractions in the oesophageal body)

High-resolution manometry in three achalasia subtypes - Harrison's Principles of Internal Medicine 22e

Subtype	Manometry Pattern
Type I (Classic)	Absent peristalsis + impaired LES relaxation; minimal oesophageal body pressurisation
Type II (With compression)	Pan-oesophageal pressurisation with all swallows
Type III (Spastic)	Premature/spastic contractions in oesophageal body

Differential Diagnosis of Achalasia:

Pseudoachalasia: tumour infiltration of gastric cardia/distal oesophagus (up to 5% of suspected achalasia); suspect with age >60, abrupt onset <1 year, significant weight loss
Chagas disease: T. cruzi infection destroying autonomic ganglia; endemic in South America
Opioid-induced oesophageal dysmotility
Distal oesophageal spasm

Treatment:

Modality	Details	Efficacy
Nitrates / Ca-channel blockers	Pre-meal; temporising only	Poor long-term
Botulinum toxin injection	Endoscopic injection into LES; inhibits ACh release	~2/3 cases respond; effect lasts ~6 months
Pneumatic balloon dilation	Non-compliant cylindrical balloon dilated to 3-4 cm across LES	60-90%; perforation risk 0.5-5%
Laparoscopic Heller myotomy	Surgical division of circular muscle of LES + partial fundoplication	62-90%; equivalent to dilation at 5 years
POEM (Peroral Endoscopic Myotomy)	Endoscopic submucosal tunnel + circular muscle division; GERD common afterward; superior to dilation at 2 and 5 years	>80%; similar to Heller
Oesophagectomy	Refractory/advanced sigmoid deformity	Last resort

Complication: Long-standing achalasia → stasis oesophagitis → oesophageal squamous cell carcinoma (small but real increased risk)

2. Distal Oesophageal Spasm (DES)

Pathophysiology: Premature (short-latency) contractions in the oesophageal body with normal LES relaxation - the key difference from spastic achalasia. Loss of inhibitory neurotransmission (nitric oxide) causes contraction to begin before the normal inhibitory phase is complete.

Clinical Features:

Intermittent dysphagia and severe chest pain (can mimic cardiac pain)
Symptoms often triggered by hot/cold liquids, emotional stress

Investigations:

Barium swallow: "corkscrew oesophagus" or "rosary bead" pattern - due to spastic circular muscle contractions

Corkscrew oesophagus on barium swallow in distal oesophageal spasm - the helical array of contracted circular muscle creates the characteristic appearance

Classic "corkscrew oesophagus" on barium swallow in DES - Harrison's Principles of Internal Medicine 22e

Manometry: simultaneous (non-peristaltic), premature contractions in >20% of swallows with normal LES relaxation (integrated relaxation pressure <15 mmHg)

Treatment: Nitrates, calcium channel blockers, hydralazine, botulinum toxin, anxiolytics; POEM or surgical myotomy for severe refractory cases only.

3. Hypercontractile (Jackhammer) Oesophagus

Also called nutcracker oesophagus (older term for a related entity).

Definition: Extraordinarily vigorous peristaltic contractions with normal onset and latency - unlike DES where contractions are premature.

Manometry: Distal contractile integral (DCI) >8000 mmHg·s·cm in ≥20% of swallows; LES relaxation is normal.

Clinical Features: Severe chest pain, dysphagia

Treatment: Same as DES - calcium channel blockers, nitrates, botulinum toxin; POEM in refractory cases.

4. Secondary Motility Disorders

Disease	Mechanism	Pattern
Scleroderma	Smooth muscle fibrosis and atrophy → aperistalsis + incompetent LES	Severe GERD, oesophagitis, stricture
Chagas disease	T. cruzi destroys myenteric ganglia (similar to achalasia)	Manometric achalasia pattern
Diabetes mellitus	Autonomic neuropathy	Hypomotility, delayed transit
Opioid use	Mu-receptor activation → impaired LES relaxation	Pseudoachalasia-like pattern
Connective tissue disorders (mixed, SLE, polymyositis)	Variable myopathy/neuropathy	Hypomotility

Summary Comparison of Primary Motility Disorders

Feature	Achalasia	Distal Oesophageal Spasm	Hypercontractile Oesophagus
LES relaxation	Impaired	Normal	Normal
Peristalsis	Absent	Premature contractions (>20%)	Vigorous (high DCI)
Barium	Bird-beak, dilated	Corkscrew	Often normal
Main symptom	Dysphagia (solid + liquid)	Chest pain > dysphagia	Chest pain > dysphagia
Definitive treatment	POEM / Heller myotomy	CCBs / POEM if refractory	CCBs / POEM if refractory

Sources: Scott-Brown's Otorhinolaryngology Head & Neck Surgery Vol. 3 (Anatomy of the Oesophagus); Sleisenger and Fordtran's Gastrointestinal and Liver Disease (Anatomy and Histology); Harrison's Principles of Internal Medicine 22e (Motility Disorders); Robbins Pathologic Basis of Disease; Costanzo Physiology 7th Ed.

Tracheosophageal fistula

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Tracheoesophageal Fistula (TEF)

Definition

A tracheoesophageal fistula (TEF) is an abnormal communication between the trachea and the oesophagus. It is most commonly congenital but can also be acquired. When congenital, it frequently occurs alongside oesophageal atresia (EA) - a condition where the oesophagus ends in a blind pouch rather than connecting to the stomach.

Incidence: 1 in 3,000-4,500 live births
More common in males
Most common congenital anomaly of the lower respiratory tract

Embryology

The oesophagus and trachea develop from a common foregut tube. During the 4th-5th week of gestation, paired tracheoesophageal folds grow medially and fuse to form the tracheoesophageal septum, dividing the tube into:

Ventral: larynx, trachea, and lungs
Dorsal: pharynx and oesophagus

TEF results from incomplete fusion of these folds → defective septum → persistent communication between trachea and oesophagus.

A defect in the Sonic Hedgehog (SHH) signalling pathway has been implicated in animal models.

Classification (Gross Classification)

Five types of oesophageal atresia and tracheoesophageal fistula shown in order of frequency: Type C (87%), Type A (8%), Type E/H (4%), Type B (<1%), Type D (<1%)

The five types of EA/TEF in order of frequency - Barash Clinical Anaesthesia 9e

Gross Type	Description	Incidence
Type A	Isolated oesophageal atresia - NO fistula; both ends blind; gasless abdomen on X-ray	~8%
Type B	Proximal TEF + distal oesophageal atresia (proximal blind pouch connects to trachea; distal segment atretic)	<1%
Type C	Most common - Proximal blind pouch (oesophageal atresia) + distal TEF connecting lower oesophagus to trachea near carina; gas-filled abdomen on X-ray	~85-87%
Type D	Oesophageal atresia with both proximal and distal fistulae	<1%
Type E (H-type)	TEF without oesophageal atresia - oesophagus patent; fistula runs obliquely like letter "H"; diagnosis often delayed until childhood/adulthood	~3-4%

The H-type (Type E) fistula is the only type that may escape neonatal diagnosis - it presents later with recurrent chest infections and bronchiectasis.

Associated Anomalies

Up to 50% of TEF patients have other congenital anomalies. The most important associations:

VACTERL Association

Letter	Anomaly
V	Vertebral anomalies
A	Anal atresia (imperforate anus)
C	Cardiac defects (most important for prognosis; 15-25% of cases)
TE	Tracheoesophageal fistula / Oesophageal atresia
R	Renal anomalies
L	Limb defects

CHARGE Association

Coloboma, Heart defects, Atresia of choanae, Retardation of growth, Genital and urinary abnormalities, Ear abnormalities

Chromosomal Anomalies

Trisomy 18 more commonly associated than Trisomy 21
Overall chromosomal abnormality incidence: 6-10%

Pathophysiology

In Type C (most common):

The proximal blind oesophageal pouch cannot carry swallowed amniotic fluid to the stomach → polyhydramnios in utero
After birth: saliva and feeds pool in the blind pouch → overflow aspiration
The distal fistula connects the trachea to the stomach → gastric reflux passes directly into the lungs → aspiration pneumonitis / pneumonia
Positive-pressure ventilation inflates the stomach through the fistula → gastric distension + reduced FRC

In Type E (H-type):

Oesophagus is patent, but oblique fistula allows small amounts of food/liquid to enter the trachea with each swallow
Presents with chronic aspiration and recurrent pneumonia

Clinical Features

Antenatal

Polyhydramnios (fetus cannot swallow amniotic fluid in EA types)
Absent stomach bubble on prenatal ultrasound

Neonatal (Types A-D)

Feature	Mechanism
Excessive drooling / frothy oral secretions	Blind pouch overflows
Choking and coughing with first feed	Aspiration from pouch
Cyanotic episodes during feeding	Aspiration / airway compromise
Respiratory distress	Aspiration pneumonitis, gastric distension
Inability to pass NG tube beyond ~10 cm	Tube coils in blind pouch
Regurgitation of all feeds	Blind pouch has no exit

Delayed Presentation (H-type TEF)

Recurrent aspiration pneumonia
Chronic cough (especially with feeds)
Choking on feeds
Bronchiectasis in late cases
Can present in childhood or even adulthood

Diagnosis

Prenatal

Ultrasound: polyhydramnios, absent or small stomach bubble (not reliable alone)
MRI: better anatomical delineation of blind pouch

Postnatal

1. Failure to pass NG tube

10-12 Fr catheter fails to advance beyond ~10 cm from lips
Tube coils in the oesophageal pouch on chest X-ray

2. Plain Chest X-ray

Coiled NG tube in blind pouch
Gas-filled abdomen = distal TEF present (Type C)
Gasless abdomen = no distal fistula (Type A - pure atresia)
Air in proximal pouch
Evidence of aspiration pneumonitis (especially right upper lobe)
Anterior bowing of trachea from distended pouch

3. Contrast Oesophagogram / Barium Swallow

Demonstrates the pouch and any fistulous connection
"Pullback" oesophagram used for H-type: NG tube inserted deep into oesophagus, pulled back slowly while contrast injected under fluoroscopy - fistula opacifies
Small amounts of water-soluble contrast used (not barium, due to aspiration risk)

4. Rigid Bronchoscopy (Gold Standard for fistula localisation)

Directly visualises the fistula opening on the posterior tracheal wall
For H-type: NG tube advanced into distal oesophagus + air injected forcefully while bronchoscopist looks for bubbles emerging from fistula site
Alternatively, Fogarty catheter inflated in oesophagus and slowly withdrawn while inspecting posterior tracheal wall

5. Endoscopy

Useful when contrast studies are equivocal
Useful for diagnosis of recurrent/missed fistulae post-repair

6. Echocardiogram

Mandatory pre-operatively to detect congenital heart disease and right-sided aortic arch

7. Abdominal ultrasound

Screen for renal anomalies

Prognostic Classification

Waterston Classification (1962) - based on birth weight, pneumonia, associated anomalies

Group	Criteria	Survival
A	BW >2.5 kg, healthy	~99%
B	BW 1.8-2.5 kg OR higher BW with moderate pneumonia/moderate anomaly	~95%
C	BW <1.8 kg OR any weight with severe pneumonia/severe cardiac anomaly	~60-71%

Spitz Classification (1994) - simpler, still widely used

Group	Criteria	Mortality
I	BW >1500 g, no major cardiac defect	~2%
II	BW <1500 g OR major cardiac defect	~11-22%
III	BW <1500 g AND major cardiac defect	High

Main prognostic factors: cardiac anomaly (most important), birth weight, length of gap, and associated anomalies.

Management

Pre-operative Stabilisation

Keep infant prone/head-up position (30-45°) - reduces reflux into lungs
Replogle tube (double-lumen sump catheter) in blind ouch with continuous suction to prevent overflow aspiration
Withhold oral feeds
IV fluids and electrolyte correction
Treat pneumonia with antibiotics
Echocardiogram and renal USS
Vitamin K administration

Surgical Repair

Standard approach:

Right extrapleural posterolateral thoracotomy (or thoracoscopic VATS - increasingly preferred)
Identify and ligate/divide the fistula at the trachea
Primary end-to-end oesophageal anastomosis
Repair ideally within 24-48 hours if infant is stable

Long-gap oesophageal atresia (gap >3 cm or height of 2 vertebrae):

Foker technique: external traction sutures applied to both ends of oesophagus through the chest wall, gradually tensioned over days-weeks to lengthen the oesophagus before anastomosis
Colonic interposition or gastric pull-up if lengthening fails
Free jejunal graft as alternative conduit

H-type fistula: cervical approach (right-sided neck incision) sufficient in most cases; endoscopic cauterisation/trichloroacetic acid ablation increasingly reported

Anesthetic Considerations

Aim to avoid positive-pressure mask ventilation before fistula is controlled (gastric distension risk)
Inhalational induction preferred with spontaneous ventilation until fistula is ligated
ETT placed distal to the fistula opening (bronchoscopy first to identify fistula location)
Balloon embolectomy catheter can occlude the fistula temporarily during induction
Invasive arterial monitoring recommended (mediastinal manipulation causes haemodynamic instability)

Complications

Early Post-operative

Complication	Details
Anastomotic leak	Most common early complication; presents with pneumothorax or mediastinitis
Recurrent TEF	~5-20% recurrence rate; usually at anastomotic site
Oesophageal stricture	At anastomosis; requires serial dilatation
Pneumonia/aspiration	From residual dysmotility or leaks

Late Complications

Complication	Details
Gastro-oesophageal reflux (GERD)	Very common; often severe; may require fundoplication
Tracheomalacia	Weak anterior tracheal wall (shared with oesophagus developmentally); presents with "TOF cough" - harsh, barking cough
Oesophageal dysmotility	Persistent; only 20% have normal pulmonary function at long-term follow-up
Growth failure	Up to 50% below 25th percentile for weight in first 5 years
Barrett's oesophagus	From chronic GERD

Acquired TEF

Occurs in adults from:

Malignancy (>50% of acquired TEFs): oesophageal/lung cancer eroding into the trachea
Iatrogenic: tracheostomy cuff pressure necrosis, endotracheal intubation, prolonged NG tube use
Trauma: penetrating neck/chest injury
Infection: TB, mediastinitis
Post-radiotherapy necrosis

Management: Endoscopic stenting (oesophageal ± tracheal stents) for malignant TEF (palliative); surgical repair for benign acquired TEF. Median survival without treatment ~3 months for malignant TEF.

Summary Table

Type	Anatomy	Incidence	Presentation	X-ray
C	EA + distal TEF	85-87%	Neonatal, cyanosis, choking	Gas-filled abdomen
A	Isolated EA, no fistula	~8%	Neonatal, drooling	Gasless abdomen
E/H	TEF only, no EA	~3-4%	Delayed - recurrent chest infections	Normal bowel gas
B	Proximal TEF + distal EA	<1%	Neonatal + pneumonia	Gasless abdomen
D	EA + both fistulae	<1%	Neonatal + severe pneumonia	Variable

Sources: Cummings Otolaryngology Head & Neck Surgery; The Developing Human (Moore & Persaud); Sleisenger & Fordtran's Gastrointestinal and Liver Disease; Barash Clinical Anaesthesia 9e; Miller's Anaesthesia 10e; K.J. Lee's Essential Otolaryngology; Tintinalli's Emergency Medicine

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